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Short term control of blood pressure
Neuronal control (short term) of blood pressure: Anatomy: Baroreceptors are present in carotid sinus and aorta. Stretching of these receptors, (due to increasing blood pressure) increases afferent signals to medulla. Contracting of these sinuses, causes contracting of the baroreceptors and decreases signals sent to medulla. Carotid sinus baroreceptors send AFFERENT nerves VIA the 9th cranial nerve (glossopharyngeal nerve) using the carotid sinus nerve to the medulla. Aortic baroreceptors send AFFERENT nerves via 10th cranial nerve (vagus) to the medulla. Physiology: The Central regulator in the medulla that coordinates the response to changes in Blood pressure is called the NUCLEUS OF TRACTUS SOLITARIUS. (just a structure in the medulla). When this structure receives information from the baroreceptors, it sends signals to THREE more structures in the medulla. These are the cardio inhibitory center, the cardio acceleratory center and the vasomotor center. When blood pressure increases, signals to the nucleus of Tractus Solitarius (NTS) causes it to stimulate the cardio inhibitory center in the medulla. This in turn sends signals via the right vagus nerve, back to the Sino Atrial node in the heart. This is a parasympathetic innervation (using Acetyl choline) which serves to act on muscarinic receptors in the SA node to decrease their activity. This reduces cardiac output which reduces Blood pressure. At the same time, the NTS also sends an inhibitory signal to the Cardiac acceleratory center. (Inhibits Cardio acceleratory center). This is part of the sympathetic nervous system, so the inhibited signals from the cardiac acceleratory center travel DOWN the spine, (exiting via lateral horn) sending post ganglionic fibers to the SA NODE. This signal is inhibitory so it reduces the sympathetic discharge (decreasing nor adrenaline) to the SA node. In so doing it reduces the Cardiac output. Finally the NTS also sends signals to the vasomotor center in the medulla, instructing it to decrease its discharge i.e. it inhibits the vasomotor center. This is part of the sympathetic nervous system, so nerve fibers run down the spine, exit post ganglionically then go to the veins, arterioles, adrenal medulla AND juxtaglomerular apparatus of the kidneys. Inhibiting the vasomotor center, decreases sympathetic discharge to these organs. This decreases the tone of the veins and the arterioles which increases capacitance of the veins and reduces cardiac load, and decreases the peripheral arterial resistance. Together these two factors decrease the blood pressure. Reducing sympathetic discharge to adrenal medulla causes LESS release of Epinephrine systematically. This further reduces tone in the arteries and veins and decreases the general activity of the cardiac muscle; altogether reducing blood pressure. When blood pressure is falling, the opposite happens. Contraction of the carotid and aortic sinuses decreases the frequency of impulses going via afferent nerves to the NTS. This nucleus sends signals to the three medullary structures as described above. This time, the NTS signals the Cardio inhibitory center to decrease activity. Via the vagal nerve, the parasympathetic discharge decreases and Cardiac output increases. The NTS stimulates both the cardio acceleratory center and the vasomotor center to increase their activity and discharge. Via sympathetic nerves, the SA node is stimulated to increase Cardiac output. Via similar sympathetic nerves vasomotor discharge increases tone in both veins and arteries, decreasing venous pooling of blood and increasing peripheral vascular resistance. Both serve to increase blood pressure. Finally, sympathetic discharge to the adrenal medulla increases its production of circulating Epinephrine. This has a direct effect on cardiac muscle to increase chronotropic and inotropic contractions, thus increasing cardiac output. Circulating epinephrine also contributes to increasing venous and arterial tone, again increasing blood pressure. Orthostatic hypotension: In cases where blood volume is low, (cholera), despite mechanisms to increase sympathetic outflow, the constricted vein cannot squeeze sufficient blood to maintain adequate venous return. The cardiac output will NOT be corrected and vertigo ensues; a sign of hypoperfusion to the CNS. On standing, if you take blood pressure, blood pressure does not go up, it goes DOWN. Sympatholytic drugs esp those that do alpha blockade, will lead to orthostatic hypotension.